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Bruce D. McCollister, Department of Microbiology, University of Colorado Health Sciences Center, B175, Room 4615, 4200 E. 9th Ave., Denver, CO 80262, USA,
Andres Vazquez-Torres, Department of Microbiology, University of Colorado Health Sciences Center, B175, Room 4615, 4200 E. 9th Ave., Denver, CO 80262, USA
Mononuclear phagocytes associate with S. enterica early in the disease process before acute inflammatory abscesses are formed, as well as during later stages of the acquired immune response in which macrophages form part of well-organized granulomas (Mastroeni et al., 1995; Richter- Dahlfors et al., 1997). The ability to survive within macrophages is a key event in the pathogenesis of Salmonella enterica (Fields et al., 1986). A growing body of information indicates that macrophages can serve as sites for S. enterica replication, even though they can be activated to exert potent anti- S. enterica activity. The great majority of the intimate interactions between S. enterica and macrophages take place inside a specialized endocytic vacuole named the phagosome. This chapter discusses the dynamic S. enterica phagosome as it pertains to the pathogenesis of this intracellular Gram-negative bacterium.
Immunological and genetic manipulations in animal models of infection, as well as the observation of naturally occurring genetic traits, have revealed that genetic loci encoding Nramp1, TLR4, NADPH oxidase and IFNγ play key roles in resistance to S. enterica infection. These host defenses are expressed directly by macrophages or, as in the case of IFNγ, up-regulate the anti-S. enterica activity of mononuclear phagocytes. In the following sections, we will discuss both the mechanisms by which these host defenses contribute to the anti-S. enterica activity of macrophages, and the virulence factors used by S. enterica to avoid these components of the antimicrobial arsenal of professional phagocytes.
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